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Neuroradiology |
1 From the Departments of Radiology (E.A.K., S.C., G.J., A.M., I.I.K.), Neurosurgery (E.A.K., J.G.G., P.J.K.), and Pathology (D.Z., D.C.M.) and the Kaplan Comprehensive Cancer Center (E.A.K., D.Z., D.C.M., P.J.K.), New York University Medical Center, 560 First Ave, New York, NY 10016. From the 1997 RSNA scientific assembly. Received April 21, 1998; revision requested July 2; revision received August 6; accepted November 6. Address reprint requests to E.A.K.
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Abstract |
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 TOP Abstract IntroductionMATERIALS AND METHODSRESULTSDISCUSSIONReferences |
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MATERIALS AND METHODS: MR imaging was performed in 29 patients by using a first-pass gadopentetate dimeglumine T2*-weighted echo-planar perfusion sequence followed by conventional imaging. The perfusion data were processed to obtain a color map of relative regional CBV. This information formed the basis for targeting the stereotactic biopsy. Relative CBV values were computed with a nondiffusible tracer model. The relative CBV of lesions was expressed as a percentage of the relative CBV of normal white matter. The maximum relative CBV of each lesion was correlated with the histopathologic grading of astrocytomas obtained from samples from stereotactic biopsy or volumetric resection.
RESULTS: The maximum relative CBV in high-grade astrocytomas (n = 26) varied from 1.73 to 13.7, with a mean of 5.07 ± 2.79 (± SD), and in the low-grade cohort (n = 3) varied from 0.92 to 2.19, with a mean of 1.44 ± 0.68. This difference in relative CBV was statistically significant (P < .001; Student t test).
CONCLUSION: Echo-planar perfusion imaging is useful in the preoperative assessment of tumor grade and in providing diagnostic information not available with conventional MR imaging. The areas of perfusion abnormality are invaluable in the precise targeting of the stereotactic biopsy.
Index terms: Astrocytoma, 10.363, 10.3634 • Brain neoplasms, diagnosis, 10.363, 10.3634 • Brain neoplasms, MR, 10.121412, 10.121415, 10.121416, 10.12143, 10.12144 • Brain, perfusion, 10.363, 10.3634 • Magnetic resonance (MR), perfusion study, 10.12149 • Stereotaxis, 10.1267
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Introduction |
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TOPAbstractIntroductionMATERIALS AND METHODSRESULTSDISCUSSIONReferences |
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An important factor in the malignancy of astrocytomas is their ability to infiltrate the brain parenchyma. Tumor infiltration usually follows the vascular channels of the white matter tracts and spreads across the commissural fibers. This pathway allows distant tumor spread without disruption of the blood-brain barrier and with relative preservation of the underlying cytoarchitecture of the brain. Removing the infiltrated parenchyma is usually not possible without resecting functioning tissue, often in functionally very important areas of the brain (5,6). Another characteristic of malignant astrocytomas is their ability to recruit and synthesize vascular networks for further growth and proliferation. The degree of vascular proliferation is also an important parameter in determining the biologic aggressiveness and histopathologic grading of astrocytomas (7–9). It is important and necessary to assess the microvascularity of astrocytomas, and hence their malignancy and proliferative potential, as a part of treatment planning.
Conventional magnetic resonance (MR) imaging with gadolinium-based contrast agents has been useful in the characterization of brain tumors (10), but at the concentrations of contrast agents normally used, such imaging primarily depicts areas of disruption of the blood-brain barrier (with or without concomitant angiogenesis) rather than tumor vascularity per se (11,12). Contrast enhancement may be more extensive in areas of vascular hyperplasia; however, contrast enhancement does not provide quantitative assessment of microvascularity. Areas of contrast enhancement are not indicative of the most malignant portion of the tumor and should not be the only site of targeting for biopsy.
A more practical difficulty in the management of astrocytomas is related to potential diagnostic errors in the interpretation of samples from biopsy. Histopathologically, astrocytomas demonstrate considerable heterogeneity, with focal areas of more malignant features widespread among regions with a less aggressive histopathologic appearance. Ideally, the grading of astrocytomas should be based on histopathologic evaluation of specimens obtained from the most malignant portion of the tumor. A single sample from biopsy may, therefore, lead to an erroneous assessment of the tumor grade. Accurate grading of astrocytoma at stereotactic biopsy thus requires serial sampling from multiple sites within an imaging-defined lesion (5).
Recently, MR techniques have been developed for the assessment of cerebral perfusion, thus allowing the acquisition of complementary anatomic and physiologic information in a single examination. MR perfusion methods include arterial spin-tagging techniques without the use of an intravenously administered contrast agent (13–17). These techniques are, however, limited by sensitivity to motion and by low contrast-to-noise ratios and have not been used widely in the clinical setting. An alternative approach exploits the changes in signal intensity seen during the first passage of intravascular paramagnetic contrast agents. This approach has been used to create regional cerebral blood volume (CBV) maps in normal and in diseased brain tissue (18–20).
In recent studies, echo-planar imaging has been used to image the passage of the bolus of the intravascular contrast agent. Echo-planar imaging is capable of image formation in about 100 msec and thus allows superior temporal resolution in whole-brain imaging (21). With T2*-weighted echo-planar imaging, changes in signal intensity with the passage of an intravascular paramagnetic contrast agent can be calculated on a pixel-by-pixel basis. This information, although it is not the CBV itself, can be useful in assessing the regional vascularity of the brain without manipulation of the data.
The purpose of our study was twofold: (a) to determine the association of MR imaging-derived CBV values with histopathologic grading of astrocytomas and (b) to assess the potential role of MR perfusion imaging in identifying the foci of greatest vascular hyperplasia and hence improving the targeting accuracy at stereotactic biopsy.
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MATERIALS AND METHODS |
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TOPAbstractIntroductionMATERIALS AND METHODSRESULTSDISCUSSIONReferences |
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Before imaging, patients were surgically fitted with a stereotactic head frame (Compass; Compass International, Rochester, Minn), and an 18- or 20-gauge intravenous catheter was inserted in the antecubital area for contrast agent administration. Imaging was performed on a 1.5-T imager (Magnetom Vision; Siemens Medical Systems, Iselin, NJ). Localizing sagittal T1-weighted images were obtained, followed by nonenhanced axial T1-weighted (600/14 [repetition time msec/echo time msec]), intermediate–weighted (3,400/17), and T2-weighted (3,400/119) images of the brain. The location and size of the tumor and the positions of the superior and inferior margins were determined from the T2-weighted images. Dynamic contrast agent–enhanced T2*-weighted gradient-echo echo-planar imaging (1,000/54) during the first pass of a bolus of gadopentetate dimeglumine (Magnevist; Berlex, Wayne, NJ) was then performed. Finally, postcontrast axial T1-weighted images were obtained.
Perfusion-weighted imaging was performed by using a lipid-suppressed, T2*-weighted echo-planar imaging sequence with the following parameters: repetition time, 1,000 msec; echo time, 54 msec; field of view, 230 x 230 mm; section thickness, 5 or 7 mm; data matrix, 128 x 128 matrix; and in-plane voxel size, 1.8 x 1.8 mm. Between five and seven sections were obtained to cover the entire tumor volume identified on the T2-weighted images. A section gap of 0%–30% of the section thickness was used, depending on the extent of the signal intensity abnormality on the T2-weighted images. A series of 60 multisection acquisitions was acquired at 1-second intervals. The first 10 acquisitions were performed before contrast agent injection to establish a precontrast baseline. At the 10th acquisition, gadopentetate dimeglumine (0.1 mmol/kg) was injected with a power injector (Medrad, Pittsburgh, Pa) at a rate of 5 mL/sec through an 18- or 20-gauge intravenous catheter, immediately followed by a bolus injection of saline (total of 20 mL at 5 mL/sec). Several raw-data images from a single echo-planar perfusion acquisition are shown in Figure 1.
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During the first pass of the bolus of contrast agent, T2* is reduced, and hence the signal intensity on T2*-weighted images decreases. The change in relaxation rate (
R2*) (ie, the change in the reciprocal of T2*) can be calculated from the signal intensity with the following equation (20): R2*(t) = {-ln[S(t)/S0]}/TE, where S(t) is the signal intensity at time t, S0 is the precontrast signal intensity, and TE is the echo time. R2* is proportional to the concentration of contrast agent in the tissue, and CBV is proportional to the area under the curve of R2*(t), provided there is no recirculation or leakage of contrast agent (20). In general, these assumptions are violated, but the effects can be reduced by fitting a gamma-variate function to the measured R2* curve (22). This function approximates the curve that would have been obtained without recirculation or leakage. CBV can then be estimated from the area under the fitted curve rather than from the original data.
Note that the analysis outlined here does not give an absolute measurement of CBV. It is therefore usual to calculate relative CBV, the ratio of the area's CBV relative to that measured in some standard tissue, typically normal white matter.
The steps in the data analysis are therefore as follows (Fig 2): (a) Obtain curves of signal intensity against time (Fig 2, A). (b) Estimate mean precontrast signal intensity (S0) from 10 data points acquired before arrival of the bolus; it is important to exclude the first three to four images during which the steady-state MR signal is established. (c) Calculate R2*, and fit the gamma-variate function to the R2* curve (Fig 2, B). (d) Calculate the area under the fitted curve (Fig 2, C). (e) Calculate relative CBV in relation to normal white matter.
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An alternative strategy was therefore adopted. The maximum signal-intensity decrease (MSD) (Fig 2, A) was calculated for each pixel and was used to generate a color overlay for the base images. To reveal underlying anatomy, a threshold was applied so that no overlay values were calculated for white matter. In other words, MSD had to exceed some threshold value for the overlay to be calculated. Because perfusion in white matter is lower than that in other regions, careful selection of the threshold value could be used to exclude white matter. An example of an MSD map is shown in Figure 3.
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Conventional MR images were analyzed independently by two neuroradiologists (E.A.K, S.C.), with consensus if there was disagreement. These images were analyzed for the presence of contrast enhancement, perilesional signal intensity abnormality, necrosis, hemorrhage, and distant foci of signal intensity abnormality.
All biopsy specimens were analyzed independently by two neuropathologists (D.Z., D.C.M.), with consensus if there was disagreement. They had no prior knowledge of conventional or perfusion MR imaging findings. Grading of astrocytomas was based on the modified Ringertz classification: low-grade astrocytoma, anaplastic astrocytoma, or GBM (3,4). In this classification, the two most important histologic features that determine the grading of astrocytomas are cellular or nuclear pleomorphism and vascular proliferation. Necrosis must be present to make the diagnosis of GBM. The final histopathologic findings were correlated with the corresponding characteristics found at imaging, including perfusion-weighted imaging. A Student t test was used to analyze the relationship between the measured relative CBV and the histopathologic grade of astrocytomas.
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RESULTS |
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TOPAbstractIntroductionMATERIALS AND METHODSRESULTSDISCUSSIONReferences |
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Patient motion artifacts were virtually eliminated from MR images because of fixation of the head in the stereotactic frame. Magnetic susceptibility artifacts inherent to echo-planar imaging (21) were prominent at bone-air interfaces (the petrous temporal bone, skull base, and paranasal sinuses). None of the lesions studied were markedly distorted by this artifact, however. All patients tolerated the perfusion echo-planar imaging sequence without any adverse reaction to the rapid bolus injection of contrast agent. Because our group of patients was imaged immediately before surgery, all patients had an 18- or 20-gauge intravenous catheter, which allowed an injection rate of 5 mL/sec. Although not specifically asked, none of the patients complained of feelings of warmth or nausea with this aggressive bolus injection.
Table 1 summarizes the measurements of relative CBV. Measured relative CBV in the high-grade cohort (n = 26) varied from 1.73 to 13.70, with a mean of 5.07 ± 2.79 (± SD). The relative CBV in the low-grade cohort (n = 3) varied from 0.92 to 2.19, with a mean of 1.44 ± 0.68 (Table 1). This difference in relative CBV was statistically significant (P < .001). Among the patients with high-grade astrocytomas, the relative CBV in patients with GBM (n = 21) varied from 1.73 to 13.7, with a mean of 4.72 ± 2.76, whereas in patients with anaplastic astrocytomas (n = 5), relative CBV varied from 3.82 to 9.33, with a mean of 6.53 ± 2.67. This difference was not statistically significant (P = .536; Student t test). Measured values of relative CBV for the three groups are plotted in Figure 5.
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DISCUSSION |
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TOPAbstractIntroductionMATERIALS AND METHODSRESULTSDISCUSSIONReferences |
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In addition, the transformation of a low-grade tumor into a malignant form is accompanied by concomitant vascular proliferation (26). It is not known whether angiogenesis plays a triggering or permissive role in tumor dedifferentiation, but it is well recognized that the more malignant the astrocytoma, the greater the degree of vascular hyperplasia (6). The degree of neovascularization often correlates not only with biologic aggressiveness but also with the rapidity and frequency of clinical recurrence following therapy. Furthermore, the survival rate of patients with treated high-grade astrocytoma has been shown to be inversely related to the degree of vascular hyperplasia of the original tumor (27,28). Tumor angiogenesis, therefore, plays an important role in determining the biologic aggressiveness of astrocytomas and can be a crucial target in devising methods for preventing further tumor growth.
Recent developments in MR imaging have allowed the assessment of CBV and perfusion abnormalities in brain tumors (18,29). Aronen et al (18) demonstrated statistically significant differences in CBV measurements between low- and high-grade gliomas by using spin-echo echo-planar imaging. The findings from our study, in which we used gradient-echo echo-planar imaging, confirm these previous findings.
In addition, our results demonstrate the utility of color overlays of MSD for determining stereotactic biopsy targets. MSD is only indirectly related to relative CBV. However, provided the shape and length of the bolus are similar in different regions of the brain, we would expect the two to be correlated. Furthermore, MSD is much easier to calculate than relative CBV on a pixel-by-pixel basis, and this simplicity avoids the amplification of noise that can occur with more complex calculations. It is thus easier to identify "hot" areas for biopsy targeting. In all patients who underwent stereotactic biopsy in our study, biopsy samples from "hot" areas on the MSD maps showed greater vascular hyperplasia than samples from "cooler" areas. Values of relative CBV, which is clearly related to perfusion, were used for analysis as a more standard number, rather than values of MSD.
Further work is required to elucidate the relationship between MSD and relative CBV and to determine whether MSD alone might be sufficient in the future for assessing the vascularity of a given lesion. We are currently comparing MSD, relative CBV, and conventional imaging findings with histopathologic findings in patients in whom exact stereotactic sites are matched with corresponding histopathologic information.
Paramagnetic contrast agents such as gadopentetate dimeglumine are routinely used as a part of MR imaging of intracranial neoplasms (10). With conventional doses of gadolinium-based contrast agents, the primary effect a few minutes after injection is a reduction in T1. However, the relative effect on T1, T2, and T2* is a function of the concentration of the contrast agent. Note that the contrast enhancement seen on T1-weighted images is not related to the perfusion abnormality on T2*-weighted echo-planar images. Contrast enhancement in the conventional sense depicts the areas of contrast accumulation in the interstitial tissue caused by the disruption of the blood-brain barrier and not the underlying regional vascularity. During the first pass of the contrast agent, the concentration is sufficiently high to reduce T2* and, to a lesser extent, T2 (20).
We used gradient-echo echo-planar imaging, rather than spin-echo echo-planar imaging, because gradient-echo echo-planar imaging is sensitive to changes in T2* and hence gives greater signal intensity changes during the passage of the bolus. This allows detection of subtle areas of signal-intensity decrease, accentuates perfusion abnormalities within the tumor (19,20), and should improve the statistical significance of the data obtained. There are theoretic models that suggest that spin-echo methods should be more specific to small vessels such as capillaries (30), whereas gradient-echo methods will also demonstrate signal intensity changes in adjacent draining veins. However, we observed quite uniform changes throughout those areas of the brain included in the image. There was little evidence that large signal intensity changes were primarily associated with, for example, sulcal veins. This suggests that our measurements are sensitive to changes in the microvasculature even if not specific to them.
In this study, high-grade and low-grade tumors could not be differentiated accurately on the basis of the findings from conventional MR imaging. The perilesional T2 signal intensity abnormality seen in all tumors in this study is nonspecific, representing either tumor infiltration or vasogenic edema, or, more frequently, both. Furthermore, in our study, all low-grade tumors showed contrast enhancement, but almost one-fifth of GBMs did not. This observation is unusual because most low-grade glial neoplasms, except for pilocytic astrocytomas, tend not to show contrast enhancement (31). However, our low-grade lesions did not include pilocytic astrocytomas.
On the basis of the findings from our study, therefore, the presence of contrast enhancement on T1-weighted images alone cannot be used to predict the histopathologic grade of astrocytomas. The finding that the area of greatest vascular hyperplasia did not always show contrast enhancement on T1-weighted images is not surprising because conventional enhancement depends primarily on the breakdown of the blood-brain barrier. This breakdown can result either from destruction of normal capillaries by the neoplastic process or from the pathologic structure of the vascular walls of newly formed abnormal capillaries. The degree of MR perfusion abnormality, on the other hand, reflects the degree of vascular hyperplasia independent of the presence or absence of breakdown of the blood-brain barrier.
Contrast enhancement is not equivalent to perfusion abnormality. The former represents a pathologic alteration in the blood-brain barrier with or without concomitant vascular hyperplasia, whereas the degree of perfusion abnormality reflects the degree of microvascularity with or without destruction of the blood-brain barrier. If contrast enhancement were proportional to the degree of angiogenesis, there would not be any enhancement in avascular disease processes such as brain abscess, radiation necrosis, or postoperative surgical cavity, which clearly is not the case. Without the information from perfusion findings, biopsy targets would not have been accurately directed to the area of greatest vascular hyperplasia.
Although relative CBV values are not an absolute measure of regional blood volume, they reflect the degree of vascularity and may be a better indicator of the biologic aggressiveness of the tumor and, therefore, the histopathologic grade of astrocytomas. High measurements of relative CBV are more likely to correlate with high-grade tumors.
One of the shortcomings of our study is the limited number of patients with low-grade astrocytoma. This limitation is caused by the natural incidence of astrocytomas and our referral and surgical resection pattern. Low-grade astrocytomas are much less common than anaplastic astrocytomas and glioblastomas (1,32). In addition, low-grade astrocytomas may be clinically "silent" for many years before symptoms appear, whereas high-grade lesions, because of mass effect and associated vasogenic edema, tend to cause more profound symptoms and progressive neurologic deficit, warranting more urgent medical attention and imaging studies.
In conclusion, our results demonstrate the association between relative CBV measurements and the histopathologic grade of astrocytoma. These measurements allow an evaluation of the tumor grade that is not possible with conventional MR imaging. MSD maps provide a relatively simple method of obtaining functional parameters that reflect tumor vascularity. The maps are clinically useful for determining the best stereotactic biopsy site for accurate grading of the astrocytoma. At our institution, perfusion MR imaging has become a routine imaging sequence in patients suspected of having a brain neoplasm. We believe relative CBV measurements and the MSD color overlay will continue to play an important role in the preoperative management of glial neoplasms by providing noninvasive, functional information about tumor vascularity that may have a profound effect on treatment strategies and on monitoring the response to therapy.
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Footnotes |
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R2* = change in relaxation rate
ROI = region of interest Author contributions: Guarantors of integrity of entire study, E.A.K., I.I.K.; study concepts and design, E.A.K., G.J.; definition of intellectual content, E.A.K., S.C., G.J.; literature research, S.C., A.M.; clinical studies, J.G.G., P.J.K., D.Z., D.C.M.; data acquisition, S.C., A.M.; data analysis, S.C., G.J., A.M., E.A.K.; statistical analysis, S.C., A.M.; manuscript preparation, S.C., G.J., A.M.; manuscript editing, G.J., E.A.K., I.I.K.; manuscript review, E.A.K., J.G.G., I.I.K.
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TOPAbstractIntroductionMATERIALS AND METHODSRESULTSDISCUSSIONReferences |
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